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Chunk #42 — FUTURE DIRECTIONS

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Converging findings from linkage and association analyses on susceptibility genes for smoking and other addictions.
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However, it is important to acknowledge that the genetic liability accounted for by each of the 47 loci is probably less than 1% of the phenotypic variance, considering their respective effect sizes, which may also explain why they can be identified through one type of unbiased study, but not the other. Anticipating future studies on the predictive power of these loci cumulatively, we are inclined to project that the amount of heritability explained will still be limited, which renders the susceptibility map as only a beginning. Furthermore, functional studies have been conducted for limited genetic variants with certain or uncertain smoking associations (Table 4). Nevertheless, the TTC12/ANKK1-DRD2 cluster shows consistent association with smoking-related behaviors (Table 2), and the function of the most prominent variation in this region, Taq1A, still is largely unknown. 47 On the other hand, we have understood the molecular and neurobehavioral functional consequences of BDNF Met66Val polymorphism (rs6265) for more than a decade,143 although its association with ND phenotypes is still relatively weak (Table 2). Combining the susceptibility map results with relevant functional annotations will facilitate determination